Chapter 20: The Kidney Flashcards

1
Q

What is the most common and 2nd most common causes of Chronic Renal Failure (CRF) and End-Stage Renal Disease (ESRD)?

A
    • Diabetes = MOST common
    • High BP = second most common
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2
Q

What is the single most important question to ask a patient suspected of having renal disease?

Why?

A
  • - “Have you had this before?”
    • Hx of disease can imply a significantly worse prognosis or chronicity
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3
Q

What is the average size of the kidney?

A
  • 120-150 grams and continues to grow until late teens/early 20s
  • Length: 10-12 cm
  • Width: 6cm
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4
Q

How is the hilar area of the kidney different from the parenchyma?

A

Hilar, ureter and urinary bladder are lined by transitional cell epithelium

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5
Q

Why is the right kidney lower than the left?

A

Liver pushes it down

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6
Q

Where is the kidney located?

A

Renal angle: between the lower border of the 12th rib and lateral border of the erector spinae muscle.

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7
Q

If a patient comes in with kidney pain, what is its distribution?

A

Starts from renal angle and radiates forward (anterior) towards the groin.

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8
Q

How are the kidneys attached?

A
  • Fascial plane, renal artery and vein, ureter and mesentary.
  • There are NO suspensory ligments.
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9
Q

But what about the splenorenal ligament, is that a suspensory ligament that holds the kidney in place?

A

No

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10
Q

Do all small tumors form a mass?

A

NOOOO.

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11
Q

What is creatinine and in kidney dysfunctions, it is ↑ or ↓ ?

What about BUN levels?

A
  • Creatnine is a breakdown product of muscle metabolism. Usually, it is excreted NL.
    • If kidney dysfunction:
      • ↑ serum creatinine and BUN (blood urea nitrogen)
      • ↓ urine creatinine and BUN
        *
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12
Q

When is a renal biopsy performed?

A

Because of the invasivness, there must be DEFINITE indications of a kidney dysfunction.

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13
Q

What is always performed with a renal biopsy?

A

UA

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14
Q

Kidney diseases often result in edema.

What causes generalized edema vs localized edema?

A
  • Generalized edema: Heart, kidney and liver failure
  • Localized: only lung failure
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15
Q

Renal diseases can be catagorized based on what 4 compartments of the kidneys?

A
    1. Glomeruli (often immunologically mediated)
    1. Tubules (often toxic/infectious inury)
    1. Interstitium
    1. Blood vessels
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16
Q

In the kidneys,

  • DM is mainly a __________ disease.
  • Systemic HTN is mainly a _________ disease.
A
  • DM= glomerular disease
  • HTN= tubulointestinal disease (d/t vascular damage)
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17
Q

Glomerular disorders are though to be due to what?

A

Immunologic diseases (primary or secondary)

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18
Q

What is responsible for the long-term complications in diabetics?

A

Persistant hyperglycemia (glucotoxicity)

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19
Q

Azotemia

A

↑ BUN & creatinine d/t a ↓ in GFR

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20
Q

Pre-renal Azotemia

A

Azotremia d/t hypoperfusion of the kindeys (d/thypotension, shock, CHF, or cirrhosis of liver) W/O damage of the parenchyma

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21
Q

Post-renal azotemia

A

Azotremia d/t urine outflow is obstructed after leaving the kidney (distal to calyces and renal pelvis). If the obstruction is removed, azotemia is corrected.

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22
Q

Uremia

A

Azotremia + other clinical findings and signs like: metabolic, hematologic, endo, GI, neuro and CV effects

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23
Q

If Puttoff says uremia, what is the condition of the patient?

A

They are in chronic kidney diasease (CKD, same as chronic renal failure)

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24
Q

How does a patient with uremia progress and present?

How do we dx in children?

A
  • Pt has nonspecific sx, which become chronic and worse overtime as the disease worsens.
  • Dx in children is hard because of the non-specific sx.
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25
Q

Azotremia is often seen in _________ syndromes

A

Nephritic syndromes

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26
Q

Know the difference between nephrotic and nephritic syndromes

A
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27
Q

What is the NL GFR?

A

90-120 mL/min/1.73m2

Older ppl will lower GFR bc it varies w age.

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28
Q

What is acute kidney injury (AKI)/acute renal failure?

Severe cases show?

​Reversible?​

A
  • Rapid decline of GFR due to glomerular, interstitial, vascular or acute tubular injury (ATN).
    • Severe cases will show: oliguria or anuria
    • Reversible, or can progress to CKD.
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29
Q

Injury to what morphological structure of the kidney is the most common cause of Acute Kidney Injury?

A

Acute tubular injury (ATN)

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30
Q

What is Chronic Kidney Disease (CKD/Chronic Renal Failure)?

Mild/severe cases show?

Reversible?

A

Azotremia -> uremia

  • Persistantly ↓ GFR that is less than 60 mL/min/1.73 m2 for at least 3 months and/or persistent albuminuria.
    • Mild cases = clinically silent
      • Severe cases= uremia
    • Generally, irreversible
31
Q

CKD affects _____ of all adults in the US.

A

11%

32
Q

What is end-stage renal disease?

A

Less than 5% of NL GFR and the end stage of uremia.

33
Q

What is rapidly progressive glomerulonephritis (RPGN)?

A

Nephritic syndrome with rapid decline (days-weeks) in GFR, indicating severe glomerular injury.

  • Can manifest as: acute nephritis, proteinemia and acute renal failure
34
Q

Glomerular disease is often associated with what 4 main systemic disorders?

A

1. SLE

2. Diabetes

3. Amyloidosis

4. Vasculitis

35
Q

What clinical renal diseases are characterstic of tubulointestinal diseases?

A
  • 1. UTI
  • 2. Urinary tract obstruction
  • 3. Renal tumors

Renal tubular defects and acute renal failure can be both glomerular and tubulointestinal.

36
Q

What clinical renal diseases are characteristic of glomerular diseases?

A

1. Nephrotic/nephritic syndromes

2. Asymptomatic hematuria/proteinuria

3. CRF

Renal tubular defects and acute renal failure can be both glomerular and tubulointestinal.

Renal tubular defects and acute renal failure can be both glomerular and tubulointestinal.

37
Q

What are isolated urinary abnormalities?

A

Glomerular hematuria and or subnephrotic proteinuria

38
Q

What is the renal corpsucle?

A

Glomerulus and Bowmans capsule (urinary space), which captures the glomerular filtrate and sends it into the tubular system.

39
Q

Which cells of the glomerulus are contractile, phagocytic, capable of proliferation, and laying down both matrix and collagen?

A

Mesangial cells

40
Q

What is a diffuse vs. focal glomeruopathy?

A
  • Diffuse = affects ALL of the glomeruli in kidney (more than 50%)
  • Focal = not all glomeruli are affected; others are NL (less than 50%)
41
Q

What is segmental vs. global glomerulopathy?

A
  • Segmental: only PORTIONS of affected glomeruli are damaged
  • Global: the entire glomerulus is affected.
42
Q

Once any renal disease destroys nephrons and ↓ GFR to 30-50% of the normal rate, what happens?

A

Progression to ESRF occurs at a steady rate. The 2 major histological fxs are

  • 1. FSGS (focal segmental glomerulosclerosis)
  • 2. Tubulointerstitial fibrosis
43
Q

What can cause progressive glomerular injury?

A

Primary or secondary glomerular injury

44
Q

Progressive injury is due to a cycle of glomerular and nephron loss, followed by what?

A

Compensatory changes that will further cause injury and glomerulosclerosis and eventually, end-stage renal disease.

45
Q

What is the principal glomerular manifestation of progressive glomerular injury?

A

Focal segmental glomerulosclerosis, eventually leading to global glomerular involvement and glomerular obsolencence.

46
Q

The extent of damage to ___________ is MOST correlated to worsening renal function?

A

Tubulointerstitial damage,

rather than the severity of glomerular injury

47
Q

What is the pathological response of the glomerulus to injury?

What do we see in acute vs chronic injury?

A
  1. Hypercellularity of
  • -Endothelial and mesengial cells
  • -Inflammatory cells (leukocytes)
  • -Proliferation of epithelial cells & inflammatory cells => plasma proteins leaks into space => + coagulation factors => form crescents
  1. BM thickening and deposits
  2. Hyalinosis (injury of endothelium) and sclerosis (deposition of ECM)
  • Acute: hypercellularity and crescents
  • Chronic: BM thickening, hyalonisis and sclerosis
48
Q

What can be used to visualize thickening of the capillary wall?

A

Light microscopy with PAS staining

49
Q

What does electron microscopy show for basement membrane thickening?

A

Subendothelial/subepithelial deposits of immune complexes, fibrin, amyloid and increased synthesis of BM components.

50
Q

What morphological change to the glomerulus is characterized by the accumulation of homogenous/eosinophilic material under light microscopy and is typically the end result of many forms of glomerular injury?

A

Hyalinosis

51
Q

Chronic glomerular responses to injury include what 3 morphological changes?

A
  1. - Basement membrane thickening
  2. - Hyalinosis
  3. - Sclerosis
52
Q

Glomerular injury is mostly d/t immune mechanisms.

How can Ab cause injury?

A
    1. Ab react in glomerulus & ****
      * bind to ​fixed intrinsic antigens => immune complex
      * bind to planted antigens => immune complex
      • ​Can be exogenous (drugs, infections)
      • Endogenous (DNA, immunoglobulins, immune complexes)
    1. Circulating Ab-Ag complex in glomerulus
      * Endogenous
      * Exogenous
53
Q

The major cause of glomerulonephritis is what?

A

In situ immune complex formation

54
Q

What diseases are caused by in-situ formation of immune complexes?

A
  1. Anti-GBM nephrititis
  2. Membranous glomerulonephropathy
  3. Post-strep glomerulonephritis

….

55
Q

In the Heymann model of glomerulonephritis (experimental counterpart oto membranous nephropathy), Abs reacts to what Ag?

This Ag is normally found where?

A

Megalin, normally found in epithelial cell (podocyte) foot processes

56
Q

Which Ag underlies most cases of primary human membranous nephropathy?

A

M-type phospholipase A2 receptor (PLA2R)

57
Q

In membranous nephropathy, Ab binding to PLA2R in glomerular epithelial cell membranes => leads compliment activation => immune complex forms where on the BM?

Characteristic BM appearance on light microscopy?

A
  • SUBepithelial part of BM
  • THICKENED BM appearance on light microscopy
58
Q

what is the pattern of immune deposition seen in membranous nephropathy (in-situ immune complex deposition) with immunofluorescence,?

Reflects what?

A
  • GRANULAR pattern
  • d/t VERY localized antigen-AB interaction.
59
Q

What is the antigen associated with anti-GBM nephritis?

A

NC1 domain of type 4 collagen Ag

60
Q

What characteristic pattern seen with immunofluorescence in diseases caused by Abs directed against NL glomerular BM components (i.e., anti-GBM)?

A

Diffuse linear pattern bc Abs bind to intrinsic Ags along the entire legnth of GBM

61
Q

Often anti-GBM Abs cross react with other BM’s, especially where?

What syndrome does this occur in?

A
  • Lung alveoli, forming lesions in lung and kidney

- Goodpasture syndrome

62
Q

What kind of glomerular damage occurs due to anti-GBM Abs?

Leading to which clinical syndrome?

A
  • Causes severe necrotizing** and **crescentic glomerular damage
  • Leading to rapidly progressive glomerulonephritis (RPGN)
63
Q

EXOGENOUS Ags from which bacteria/viruses create circulating immune complexes leading to glomerulonephritis?

What are endogenous sources?

A
  • - Streptococcal proteins
  • - Surface Ag of HBV and viral antigens of HCV
  • - Ags of T_reponema pallidum_ and P_lasmodium falciparum_

Endogenous: SLE, IgA nephropathy

64
Q

How do highly cationic Ags vs. highly anionic Ags vs. neutral Ags differ in where they deposit and form immune-complexes form in the glomerulus?

A
  • Cationic (+) –> cross the GBM and form in subepithelial deposits
  • Anionic (-) –> dont cross GBM and form subendothelially deposits
  • Neutral charge –> tend to accumulate in the mesangium
65
Q

Immune complexes deposited in which locations of the glomerulus are more likely to be involved in an inflammatory response due to be accessible to the circulation?

A
  • Subendothelial portions of capillaries
  • Mesangial locations
66
Q

Immune complexes can form deposits:

  1. Subepithelial area (1)
  2. Epimembranous (2)
  3. Subendothelial area (3)
  4. Mesengial area (4)

Which nephropathies are most likely in each area?

A

1. Subepithelial humps (1)

  • Acute glomerulonephritis

2. Epimembranous deposits (2)

  • Membranous nephropathy

3. Subendothelial deposits (3)

  • lupus nephritis
  • membranoproliferative glomerulonephritis
  1. Mesenangial area (4)
    * IgA nephropathy
67
Q

Which coagulation factor may act as the stimulus for crescent formation associated w/ glomerular injury?

A

Thrombin

68
Q

What is the most frequent clinical presentation of Focal Segmental Glomerulosclerosis?

A
  1. Nephrotic syndrome
  2. - Nonnephrotic proteinuria
69
Q

Most common type of glomerular injury causing nephritic syndrome?

A

Immunologically mediated

70
Q

What is the difference betwene primary and secondary glomerulonephritis?

A
  • primary glomerulonephritis == disorders in which the kidney is the only/ predominant organ involved
  • secondary glomerulonephritis == when the glomerulus is affected by systemic immunologic diseases such as SLE, vascular disorders such as HTN, or m_etabolic diseases such as Fabry disease_
    • glomerular diseases are often associated with systemic disorders (e.g. _diabetes mellitu_s, SLE, vasculitis, and amyloidosis)
71
Q

________ are important for the maintenance of glomerular barrier function

A

visceral epithelial cells (i.e. podocytes);

separated from the endothelial cells by BM

72
Q
  • Diff types of glomerulopathies are characterized by one or more of four tissue changes.
    • If acute vs chronic, what changes do we see?
A
  • acute glomerular response to injury == hypercellularity and formation of crescents (if severe)
  • chronic glomerular responses to injury ==BM thickening, hyalinosis, and sclerosis
73
Q
A